Drug Database
AD

AD-201 (AD 201 / AD201)

✓ Approved

Addpharma · Small Molecule · Small Molecule

What is AD-201?

AD-201 is a small molecule developed by Addpharma. It is approved for therapeutic indications via unknown.

Drug Profile

Brand NamesAD 201, AD201
CompanyAddpharma
Drug ClassSmall Molecule
RouteUnknown
StatusApproved
Sources: ClinicalTrials.gov, Addpharma

Therapeutic Indications

AD-201 is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Vascular disordersHypertension✓ Approved
Metabolism and nutrition disordersHyperlipidaemia✓ Approved

Related Research Articles

PubMedJournal of Alzheimer's disease : JAD2026-10-16

Association between handedness and Alzheimer's disease: Results from a large MindCrowd observational study.

Chen Charles C, Huentelman Matt M, Chen Kewei K

BackgroundHandedness is tied to the lateralization of brain functions and significantly affects cognitive function and brain activity. Alzheimer's disease (AD) is a progressive brain disorder that leads to declines in memory, thinking skills, and to behavioral changes, which also exhibits lateralized patterns of brain involvement. Understanding the relationship between handedness and AD may provide useful context for interpreting findings in AD research.ObjectivePrevious findings on the relationship between AD and handedness are inconsistent.We used the large MindCrowd dataset, comprising with over 150,000 participants, study the association between AD and handedness.MethodsWe applied logistic regression models to the data with and without adjustment for other covariates to estimate the association between handedness and AD. We also performed similar analyses for samples stratified by ages. We estimated the unadjusted and adjusted odds ratios (ORs) of having AD among left- and mixed-handed participants compared with right- handed participants.ResultsOur results showed that compared with right-handed participants, left- and mixed-handed participants had higher odds of self-reported AD (the overall adjusted OR: 2.08, 95% CI: (1.69, 2.53), p < 0.001)) being larger than that for left-handers (the overall adjusted OR: 1.42, 95% CI: (1.23, 1.64), p < 0.001)). Furthermore, for each age group considered, the estimated adjusted and unadjusted ORs for mixed-handers were consistently greater than that for left-handers; all were greater than 1.0.ConclusionsOur study confirmed that there is a significant association between handedness and AD. Our findings also indicate that mixed-handedness has a stronger association with AD than left-handedness.

PMID 42885688
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PubMedAlzheimer's & dementia : the journal of the Alzheimer's Association2026-10-16

The right temperature at the right time: A framework for understanding thermoregulatory pathophysiology in Alzheimer's disease.

Blessing Esther E

The neuromodulatory subcortical system (NSS) includes thermoregulatory neurons that maintain core body temperature (Tb) and brain temperature within a narrow, diurnally varying range. Cellular pathways in NSS neurons implicated in Alzheimer's disease (AD) may be vulnerable to Tb rhythm disturbance because of their sensitivity to temperature and their thermoregulatory function. This review evaluates a framework for pathophysiological interactions between thermoregulation and AD anchored in the functional anatomy of thermoregulatory neurons. Findings in humans show that thermoregulatory neurons exhibit tau pathology in early AD, and abnormal Tb rhythm is seen in advanced AD. In rodents, cellular risk pathways for tau aggregation are both modulated by diurnal range temperature change and involved in thermoregulation. Further research is needed to bridge human and rodent findings, to understand how sex differences in Tb impact AD risk, and to identify modifiable causal links between Tb disturbance and pathophysiology toward improving clinical outcomes in early AD.

PMID 42885145
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PubMedInternational journal of molecular sciences2026-10-16

HMGB1 in Amyloid-Beta Pathology: Mechanistic Insights and Therapeutic Implications for Alzheimer's Disease.

Seol Song-I SI, Kim Ji-Eun JE, Davaanyam Dashdulam D, Park So-Young SY et al.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of amyloid-beta (Aβ) plaques and neurofibrillary tangles. Beyond these hallmark pathological features, the complex pathogenesis of AD involves cellular dysfunctions associated with chronic oxidative stress and neuroinflammation. Central to these inflammatory pathways is the extracellular release of the nuclear protein high-mobility group box 1 (HMGB1) from neurons and microglia. Extracellular HMGB1 disrupts homeostatic and reparative microglial functions, impairing the phagocytic clearance of amyloid-beta and driving neuroinflammation to accelerate AD pathogenesis. Consequently, targeting HMGB1 offers a promising therapeutic strategy for AD. This review examines recent progress and key insights regarding HMGB1-associated neuroinflammatory pathology in AD. We evaluate its regulation across transcriptional upregulation, cellular redistribution, age-related alterations, and Aβ-associated pathology. We further detail the pleiotropic effects of extracellular HMGB1, including neuroinflammation, defective Aβ phagocytic clearance, and genomic instability. Finally, we discuss the potential clinical utility of targeting HMGB1 to mitigate AD progression and provide HMGB1-related perspectives for future studies.

PMID 42883925
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PubMedInternational journal of molecular sciences2026-10-16

Distinct Superficial Epidermal Expression Patterns of IL-19 and IL-37 in Atopic Dermatitis.

Zaryczańska Anna A, Sitko Krzysztof K, Tukaj Stefan S, Trzeciak Magdalena M

Atopic dermatitis (AD) is characterized by heterogeneous immune activation extending beyond clinically apparent lesions. Interleukin-19 (IL-19) has been implicated in cytokine-responsive keratinocyte activation, whereas interleukin-37 (IL-37) has endogenous anti-inflammatory functions. Their superficial epidermal expression patterns in lesional and clinically non-lesional AD skin have not been extensively characterized within the same cohort. To compare IL19 and IL37 mRNA expression in lesional and clinically non-lesional, lesion-adjacent AD skin with healthy control skin and to explore associations between transcript abundance and clinical characteristics. In this exploratory cross-sectional study, tape strip samples were collected from lesional and clinically non-lesional skin of 32 patients with AD and from corresponding skin of 35 healthy controls. IL19 expression did not differ significantly among healthy control, lesional, and clinically non-lesional AD skin in the overall cohort. In contrast, IL37 transcript abundance was significantly higher in lesional AD skin than in healthy control skin (p = 0.0002) and was also increased in clinically non-lesional skin (p = 0.0387). In severity-stratified analyses, lesional IL37 expression was increased in both moderate and severe-to-very severe AD, whereas lower lesional IL19 expression relative to healthy control skin was observed in severe-to-very severe AD (p = 0.0412). Lesional IL19 expression showed an inverse association with EASI severity category (p = 0.045), while lesional IL37 expression was positively associated with sleep-disturbance scores (p = 0.0203). The two transcripts showed distinct expression patterns in this cohort. Increased IL37 mRNA was compatible with, but did not establish, a compensatory response extending into lesion-adjacent clinically non-lesional skin. Overall IL19 upregulation was not detected, and lower lesional expression was observed in severe-to-very severe AD. However, these exploratory observations do not establish cytokine function or validate either transcript as a stand-alone biomarker.

PMID 42883983
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PubMedJournal of Alzheimer's disease : JAD2026-10-16

Locus coeruleus degeneration impairs forebrain arteriole physiology and perfusion in a rat model of Alzheimer's disease.

Gifani Mahsa M, Chambers Laura C LC, Fernandez Zachary Z, Beck John S JS et al.

The locus coeruleus (LC) provides forebrain norepinephrine (NE) and degenerates early in Alzheimer's disease (AD). We have shown that experimental LC lesions in the Tg344-19 AD rat model result in parenchymal arteriole (PA) stenosis, blood-brain barrier permeability, amyloid angiopathy, and cognitive impairment. Here, we show that PAs from LC-lesioned Tg344-19 AD rats displayed increased myogenic tone and decreased responsiveness to TRPV4 channel agonists, which was reversible by NE replacement. MRI studies indicated reduced forebrain perfusion and fractional anisotropy in LC-lesioned animals compared to controls. Targeting LC-mediated effects on cerebral hemodynamics presents a compelling AD therapeutic target.

PMID 42885665
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PubMedTranslational vision science & technology2026-10-16

Multimodal Retinal Imaging Correlates With Brain Atrophy and Plasma Biomarkers in Alzheimer's Disease.

Luan Xiaoqian X, Shen Jianing J, Wang Youjie Y, Qiu Huihua H et al.

To investigate retinal structural and microvascular changes in Alzheimer's disease (AD) and evaluate their associations with neuroimaging markers, plasma biomarkers, and cognitive impairment. This cross-sectional study included 181 participants (95 with AD and 86 cognitively unimpaired controls). AD diagnosis was established according to National Institute on Aging-Alzheimer's Association criteria with positive amyloid-β positron emission tomography imaging. Retinal structure and microvasculature were assessed using swept-source optical coherence tomography (OCT) and OCT angiography (OCTA). Cortical thickness and gray matter volume were quantified using structural magnetic resonance imaging. Plasma Aβ42 and phosphorylated tau-217 (p-tau217) were measured, and cognitive function was evaluated using the Mini-Mental State Examination and Montreal Cognitive Assessment (MoCA). Compared with controls, patients with AD demonstrated reduced retinal nerve fiber layer, ganglion cell-inner plexiform layer (GCIPL), inner nuclear layer, and outer retinal layer thicknesses, together with lower superficial vascular complex (SVC) and deep vascular complex densities (all P < 0.001). GCIPL thickness and SVC density were associated with cortical atrophy in AD-vulnerable regions, including temporal, parietal, and occipital cortices. Lower plasma Aβ42 levels were associated with reduced retinal layer thickness and vascular density, whereas higher p-tau217 levels were associated with reduced outer retinal layer thickness and SVC density. GCIPL thickness showed the strongest association with cognitive performance, while lower SVC density was associated with poorer MoCA scores. APOE ε4 carriers exhibited greater GCIPL thinning, reduced retinal vascular density, and more extensive cortical abnormalities despite similar plasma Aβ42 and p-tau217 levels. Retinal neuronal and microvascular alterations are associated with AD-related molecular pathology, cerebral neurodegeneration, APOE ε4-related vulnerability, and cognitive impairment. OCT/OCTA may provide a noninvasive adjunct approach for characterizing neurodegenerative and neurovascular changes in AD. Retinal imaging may provide a scalable and noninvasive approach for detecting and monitoring AD pathology.

PMID 42885984
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